Focal MR spectroscopy of hippocampal CA-1 lesions in transient global amnesia.
Neurology 2008 March 26
OBJECTIVE: The pathomechanisms of transient global amnesia (TGA) remain enigmatic. Focal MR signal diffusion changes in the CA-1 sector of the hippocampus have been described in transient global amnesia, but the pathophysiologic correlate of these lesions is unknown.
METHODS: We studied the metabolic spectra of diffusion lesions in the CA-1 sector hippocampus of seven patients with TGA using MR spectroscopy (MRS) between 24 and 72 hours after onset and 2 to 5 months later. The amnestic deficit was studied using a neuropsychometric test battery.
RESULTS: Four out of seven patients with an acute TGA showed a diffusion lesion with a corresponding T2 lesion in the CA-1 sector of the hippocampus. Selective hippocampal MRS of diffusion lesions showed a lactate peak in three of four patients, but not in patients without a diffusion lesion. The NAA/creatine ratio was normal.
CONCLUSION: Lactate as a marker of anaerobic glycolysis indicates acute metabolic stress of CA-1 neurons in TGA whereas long-term neuronal metabolic changes are not found. This implies that the acute effect on hippocampal CA-1 neurons is the functional correlate of a transient global amnesia reflecting a transient perturbation of memory relevant circuits in the hippocampus.
METHODS: We studied the metabolic spectra of diffusion lesions in the CA-1 sector hippocampus of seven patients with TGA using MR spectroscopy (MRS) between 24 and 72 hours after onset and 2 to 5 months later. The amnestic deficit was studied using a neuropsychometric test battery.
RESULTS: Four out of seven patients with an acute TGA showed a diffusion lesion with a corresponding T2 lesion in the CA-1 sector of the hippocampus. Selective hippocampal MRS of diffusion lesions showed a lactate peak in three of four patients, but not in patients without a diffusion lesion. The NAA/creatine ratio was normal.
CONCLUSION: Lactate as a marker of anaerobic glycolysis indicates acute metabolic stress of CA-1 neurons in TGA whereas long-term neuronal metabolic changes are not found. This implies that the acute effect on hippocampal CA-1 neurons is the functional correlate of a transient global amnesia reflecting a transient perturbation of memory relevant circuits in the hippocampus.
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